摘要：

We have reviewed the stages in teleost thyroid function and its regulation, from the initial biosynthesis of the TH to their eventual interaction with putative receptors.TH biosynthesis depends on an adequate plasma iodide level, determined partly by dietary iodide and partly by active branchial iodide uptake from the water, Pulse-injected radioiodide can be used to evaluate thyroidal iodide uptake, aspects of TH biosynthesis and TH thyroidal secretion. However, owing to variable plasma iodide levels, care is required in interpretating these parameters. TH biosynthesis, thyroglobulin properties and intrathyroidal secretion mechanisms have received limited recent attention. Histological indices of thyroid tissue changes, while useful in many situations, do not always correlate with more direct estimates of thyroidal secretion and can be misleading.Thyroid function is regulated by the hypothalamo-pituitary-thyroid axis, but neither the identities of the hypothalamic factors nor a reliable immunoassay for TSH have been established. Currently, activity of the hypothalamic-pituitary axis is usually determined by pituitary thyrotrope histological appearance or bioassay of pituitary TSH. Plasma free T 4 feeds back at both the pituitary and hypothalamic levels and inhibits TSH release. Thyroidal T 4 secretory activity is presumably adjusted to maintain a constant plasma T 4 level according to physiologic state.Plasma T 4 is probably the most commonly used index of thyroidal status. However, (1) T 4 is probably not the active form of TH, (2) the T 4 plasma level may be influenced by the binding properties of plasma proteins, and (3) the T 4 concentration alone makes no provision for the rate of T 4 turnover in plasma. The most practical way to measure thyroidal T 4 SR is to determine plasma T 4 DR, and assuming steady-state conditions, equate it to T 4 SR. The T 4 DR is determined from kinetic studies employing * T 4 , which also enable estimates of sizes of vascular and extravascular T 4 pools and their rates of exchange. Excretion of T 4 or its derivatives in urine or bile can be determined also. A high proportion of T 4 is enzymatically monodeiodinated in liver and other tissues, generating T 3 for local (intracellular) and vascular systemic compartments.Both in vivo and in vitro methods have been used to quantify T 4 deiodinase activity, which is highly responsive to physiologic state and environmental variables. T 3 production is inhibited by a moderate T 3 excess indicating an autoregulatory system, whereby tissue T 3 levels are maintained at a set-point appropriate for a particular physiologic state. The rate of T 3 production provides an informative measure of thyroidal status in a given tissue. However, other pathways also contribute to the maintenance of T 3 homeostasis at a particular set-point. These include the rate of T 3 degradation to 3,3′-T 2 , the rate of T 4 substrate diversion to rT 3 (an inactive isomer) and by the excretion of parent compounds or conjugates in bile and urine. Potential losses across branchial or integumentary surfaces have yet to be evaluated.The most fundamental measure of thyroidal status is represented by the amount of T 3 saturably bound to receptors/nucleus for the cell type of interest. This is estimated most accurately in double isotope studies in which T 3 contributions from both vascular and intracellular compartments are evaluated. Less satisfactory but meaningful indices of T 3 availability to receptor sites may be obtained from the plasma T 3 (or free T 3 ) level and from the tissue T 3 level. The former is appropriate if the cell type in question obtains its T 3 primarily from plasma; the latter should be measured if the cell type derives its T 3 mainly through intracellular deiodinase activity. If the proportion of vascular T 3 /intracellular T 3 bound to receptors is known, it may indicate the degree of receptor activation. However, even cytosolic T 3 levels may not vary in proportion to nuclear T 3 levels.Differences in thyroidal function betwe

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